It is proposed to study the mechanism of concomitant antitumor immunity that is generated against progressive solid tumors in syngeneic mice. This paradoxical state of immunity will be studied in terms of the kinetics of production, and the properties of the sensitized T cells that mediate it, and in terms of the way in which these cells cause the systemic activation and mobilization of macrophages. The contribution of T cells and macrophages to the expression of immunity will also be investigated. In addition, experiments will be designed to test the hypothesis that the susceptibility of large tumors to endotoxin-induced necrosis and regression depends on the prior generation by the host, of a state of concomitant immunity, because of the need for an activated macrophage system. C. parvum-potentiated, tumor specific, immunization immunity will be studied in terms of the conditions that limit the entry of the T cell effectors of this immunity into established progressive tumors.